Functional coix seed protein hydrolysates as a novel agent with potential hepatoprotective effect

The aim of this study is to explore the hepatoprotective potential of coix seed protein hydrolysates (CPP) against alcohol-induced liver injury, and investigate the underlying mechanisms.

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Cardamonin Reduces Acetaminophen-Induced Acute Liver Injury in Mice via Activating Autophagy and NFE2L2 Signaling

Frontiers in Pharmacology ◽

10.3389/fphar.2020.601716 ◽

2020 ◽

Vol 11 ◽

Author(s):

Qiushi Xu ◽

Yunhui Fan ◽

Juan J. Loor ◽

Yusheng Liang ◽

Xudong Sun ◽

...

Keyword(s):

Liver Injury ◽

Acute Liver Injury ◽

High Mobility ◽

Hepatoprotective Effect ◽

Receptor Protein ◽

Related Factor ◽

Protective Effects ◽

Toll Like Receptor 4 ◽

Sequestosome 1 ◽

Underlying Mechanisms

Cardamonin (CD), a naturally occurring chalcone derived from the Alpinia species, has been shown to exert antioxidant and anti-inflammatory activity, but its role in the prevention of acetaminophen- (APAP-) induced hepatotoxicity remains elusive. The objective of this study was to determine the protective effects of CD against APAP-induced acute liver injury (ALI) and the underlying mechanisms. Wild-type or transcription factor nuclear factor erythroid 2-related factor 2- (NFE2L2-) deficient mice were treated with CD (50 or 100 mg/kg, i.p.) or vehicle for 24 h. Subsequently, these mice were challenged with APAP (400 mg/kg, i.p.) for 6 h. Liver and blood samples were collected to evaluate liver injury and protein abundance. Treatment with CD significantly reduced APAP-induced hepatotoxicity. Furthermore, CD effectively reduced APAP-induced inflammation by inhibiting high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and NOD-like receptor protein 3 (NLRP3) signaling. In addition, CD induced activation of sequestosome 1 (p62) and NFE2L2 signaling and facilitated autophagy. By applying autophagy inhibitor 3-methyladenine (3-MA; 20 mg/kg, i.p.), further mechanistic exploration revealed that NFE2L2 deficiency promoted autophagic activity induced by CD treatment, which was conducive to the hepatoprotective effect of CD against APAP-induced hepatoxicity in NFE2L2−/− mice. Overall, data suggest that CD has hepatoprotective effect against APAP-induced ALI, which might contribute to the activation of NFE2L2 and autophagy.

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Scutellarin Ameliorated Carbon Tetrachloride-Induced Chronic Liver Injury in Mice

10.21203/rs.3.rs-60084/v1 ◽

2020 ◽

Author(s):

Zhimin Miao ◽

Yingying Zhao ◽

Chunyan Li ◽

Lingmin Chen ◽

Jianeng Zhou ◽

...

Keyword(s):

Carbon Tetrachloride ◽

Liver Injury ◽

Function Analysis ◽

Chronic Liver ◽

Hepatoprotective Effect ◽

Mrna Levels ◽

Chronic Liver Injury ◽

Tnf Α ◽

Anti Oxidant ◽

Underlying Mechanisms

Abstract Background: Erigeron breviscapus (Vant.) Hand. -Mazz. is an edible and traditional medical herb and its extract scutellarin (SCU) is a widely used flavonoid showing anti-oxidant and anti-inflammatory activities. The purpose of this study was to evaluate the hepatoprotective effect of SCU on carbon tetrachloride (CCl4)-induced chronic liver injury in mice and reveal the underlying mechanisms. Methods: Chronic liver injury in mice was induced by intraperitoneal injection of 1 ml/kg CCl4 every three days. SCU (15 mg/kg, 30 mg/kg and 60 mg/kg) was administered through gavage every day. Bifendate (120 mg/kg) serves as a positive drug to validate the effectiveness of SCU.Results: The hepatoprotective effect of SCU was confirmed by liver function analysis, histological analysis and TUNEL assay. Administration of SCU recovered the activities of superoxide dismutase (SOD) and reduced the production of malondialdehyde (MDA). Additionally, treatment with SCU significantly decreased the mRNA levels of pro-inflammatory cytokines including IL-6, IL-1β and TNF-α. Moreover, SCU treatment suppressed the activation of NF-κB by decreasing the degradation of IκBα and inhibited the expression of CYP2E1. The 16S rRNA sequencing demonstrated that intake of SCU significantly remodeled gut microbiota, especially enriching the following: Lactobacillus, Coprobacillus, Akkermansia, Bifidobacterium, Parabacteroides. Conclusion: Our findings showed that SCU effectively ameliorated CCl4-induced chronic liver injury. This hepatoprotective effects might be attributed to inhibition of CCl4-induced NF-κB and CYP2E1 activation and enrichment of beneficial microbial community.

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Hepatoprotective effect of anemoside B4 against sepsis-induced acute liver injury through modulating the mTOR/p70S6K-mediated autophagy

Chemico-Biological Interactions ◽

10.1016/j.cbi.2021.109534 ◽

2021 ◽

pp. 109534

Author(s):

Liang Pei ◽

Linxi He

Keyword(s):

Liver Injury ◽

Acute Liver Injury ◽

Hepatoprotective Effect

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Mesenchymal stromal cell-derived exosome-rich fractionated secretome confers a hepatoprotective effect in liver injury

Stem Cell Research & Therapy ◽

10.1186/s13287-017-0752-6 ◽

2018 ◽

Vol 9 (1) ◽

Cited By ~ 37

Author(s):

Apeksha Damania ◽

Deepika Jaiman ◽

Arun Kumar Teotia ◽

Ashok Kumar

Keyword(s):

Liver Injury ◽

Mesenchymal Stromal Cell ◽

Stromal Cell ◽

Hepatoprotective Effect

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Hepatoprotective effect of a curcumin/absinthium compound in experimental severe liver injury

Chinese Journal of Digestive Diseases ◽

10.1046/j.1443-9573.2003.00133.x ◽

2003 ◽

Vol 4 (3) ◽

pp. 122-127 ◽

Cited By ~ 2

Author(s):

F MAROTTA ◽

YR SHIELD ◽

T BAMBA ◽

Y NAITO ◽

E MINELLI ◽

...

Keyword(s):

Liver Injury ◽

Hepatoprotective Effect ◽

Severe Liver

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Amaranth seed protein hydrolysates have in vivo and in vitro antihypertensive activity

Food Chemistry ◽

10.1016/j.foodchem.2010.11.065 ◽

2011 ◽

Vol 126 (3) ◽

pp. 878-884 ◽

Cited By ~ 68

Author(s):

Mariana Fritz ◽

Bruno Vecchi ◽

Gustavo Rinaldi ◽

María Cristina Añón

Keyword(s):

Seed Protein ◽

Protein Hydrolysates ◽

Antihypertensive Activity ◽

Amaranth Seed

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Apocynum venetum Attenuates Acetaminophen-Induced Liver Injury in Mice

The American Journal of Chinese Medicine ◽

10.1142/s0192415x15500299 ◽

2015 ◽

Vol 43 (03) ◽

pp. 457-476 ◽

Cited By ~ 12

Author(s):

Wenyan Xie ◽

Chen Chen ◽

Zhihui Jiang ◽

Jian Wang ◽

Matthias F. Melzig ◽

...

Keyword(s):

Liver Injury ◽

Histopathological Examination ◽

Folk Medicine ◽

Analgesic Drug ◽

Once Daily ◽

Apocynum Venetum ◽

Anti Oxidant ◽

Underlying Mechanisms ◽

Serum Aminotransferases ◽

Hepatocyte Death

Apocynum venetum L. (A. venetum) has long been used in oriental folk medicine for the treatment of some liver diseases; however, the underlying mechanisms remain to be fully elucidated. Acetaminphen (APAP) is a widely used analgesic drug that can cause acute liver injury in overdose situations. In this study, we investigated the potential protective effect of A. venetum leaf extract (ALE) against APAP-induced hepatotoxicity. Mice were intragastrically administered with ALE once daily for 3 consecutive days prior to receiving a single intraperitoneal injection of APAP. The APAP group showed severe liver injury characterized by the noticeable fluctuations in the following parameters: serum aminotransferases; hepatic malondialdehyde (MDA), 3-nitrotyrosine (3-NT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH). These liver damages induced by APAP were significantly attenuated by ALE pretreatments. A collective analysis of histopathological examination, DNA laddering and western blot for caspase-3 and cytochrome c indicated that the ALE is also capable of preventing APAP-induced hepatocyte death. Hyperoside, isoquercitrin and their derivatives have been identified as the major components of ALE using HPLC-MS/MS. Taken together, the A. venetum possesses hepatoprotective effects partially due to its anti-oxidant action.

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Hepatoprotective Effect of Polysaccharides Isolated from Dendrobium officinale against Acetaminophen-Induced Liver Injury in Mice via Regulation of the Nrf2-Keap1 Signaling Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/6962439 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 12

Author(s):

Guosheng Lin ◽

Dandan Luo ◽

Jingjing Liu ◽

Xiaoli Wu ◽

Jinfen Chen ◽

...

Keyword(s):

Liver Injury ◽

Signaling Pathway ◽

Nuclear Translocation ◽

Hepatoprotective Effect ◽

Dendrobium Officinale ◽

Regulatory Subunit ◽

Heme Oxygenase 1 ◽

Related Factor ◽

Glutamate Cysteine Ligase ◽

Nrf2 Signaling Pathway

The effect of polysaccharides isolated from Dendrobium officinale (DOP) on acetaminophen- (APAP-) induced hepatotoxicity and the underlying mechanisms involved are investigated. Male Institute of Cancer Research (ICR) mice were randomly assigned to six groups: (1) control, (2) vehicle (APAP, 230 mg/kg), (3) N-acetylcysteine (100 mg/kg), (4) 50 mg/kg DOP, (5) 100 mg/kg DOP, and (6) 200 mg/kg DOP. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the serum and glutathione (GSH), malondialdehyde (MDA), catalase (CAT), total antioxidant capacity (T-AOC), myeloperoxidase (MPO), and reactive oxygen species (ROS) levels in the liver were determined after the death of the mice. The histological examination of the liver was also performed. The effect of DOP on the Kelch-like ECH-associated protein 1- (Keap1-) nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway was evaluated using Western blot analysis and real-time polymerase chain reaction (PCR). The results showed that DOP treatment significantly alleviated the hepatic injury. The decrease in ALT and AST levels in the serum and ROS, MDA, and MPO contents in the liver, as well as the increases in GSH, CAT, and T-AOC in the liver, were observed after DOP treatment. DOP treatment significantly induced the dissociation of Nrf2 from the Nrf2−Keap1 complex and promoted the Nrf2 nuclear translocation. Subsequently, DOP-mediated Nrf2 activation triggered the transcription and expressions of the glutamate–cysteine ligase catalytic (GCLC) subunit, glutamate–cysteine ligase regulatory subunit (GCLM), heme oxygenase-1 (HO-1), and NAD(P)H dehydrogenase quinone 1 (NQO1) in APAP-treated mice. The present study revealed that DOP treatment exerted potentially hepatoprotective effects against APAP-induced liver injury. Further investigation about mechanisms indicated that DOP exerted the hepatoprotective effect by suppressing the oxidative stress and activating the Nrf2−Keap1 signaling pathway.

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